Myocardial ischemia/reperfusion (MI/R) injury usually occurs in patients with cardiovascular disease. However, myocardial reperfusion insult often induces apoptosis. It is assumed that that microRNAs (miRNAs) are involved in the pathological and physiological processes associated with myocardial ischemia/reperfusion (MI/R). In the present study, we found decreased expression of miR-342-5p in hypoxia/reoxygenation (H/R) cardiomyocyte model (H9C2 cells) and MI/R mouse model. Alternatively, overexpression of miR-342-5p was found to ameliorate myocardial cell damage in both and . In addition, G protein-coupled receptor, family C, group 5, member A (GPRC5A) was identified as a direct target of miR-342-5p. The up-regulation of GPRC5A functioned to inhibit the previously observed protective effect of miR-342-5p in the H9C2 H/R model. Our results revealed that miR-342-5p may be a potential target for MI/R injury prevention and therapy of MI/R injury.
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http://dx.doi.org/10.1691/ph.2020.0383 | DOI Listing |
Cardiovasc Res
January 2025
State Key Laboratory of Cardiovascular Disease, Clinical Pharmacology Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.
Aims: The therapeutic efficacy of coronary revascularization is compromised by myocardial ischemia-reperfusion (MI/R) injury. Higher levels of circulating arachidonic acid (AA) are reportedly associated with lower risk of cardiovascular disease. The cyclooxygenase (COX) pathway metabolizes AA into prostaglandins (PGs) and the platelet-activating thromboxane A2 (TXA2), which is inhibited by aspirin.
View Article and Find Full Text PDFRedox Biol
December 2024
Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA; Department of Biomedical Engineering, UAB, Birmingham, AL, USA. Electronic address:
Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.
View Article and Find Full Text PDFAdv Sci (Weinh)
December 2024
Department of Cardiology, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou, 510515, China.
Ischemic preconditioning (IPC) therapy application to attenuate myocardial ischemia-reperfusion (MI/R) injury in clinical practice remains challenging. The secretome, derived from hypoxia-preconditioned cardiomyocytes (SHPC), potentially mimics the IPC microenvironment and facilitates IPC clinical translation. This study aims to determine whether SHPC can be a feasible alternative to IPC for attenuating MI/R injury, and to identify the functional factor of SHPC.
View Article and Find Full Text PDFFront Neurosci
November 2024
Department of Physiology, Shanxi Medical University, Taiyuan, China.
Objective: To investigate the effect of (+)-borneol on neuroinflammation and microglia phenotype polarization in epileptogenesis and its possible mechanism.
Methods: Based on mouse models of status epilepticus (SE) induced by pilocarpine, and treated with 15 mg/kg (+)-borneol, western-blot was used to detect the expressions of NeuN, Iba-1, TLR4, p65 and p-p65 in the hippocampus. Immunofluorescence was used to detect the expression of apoptosis-related proteins Bax and Bcl-2.
J Ginseng Res
November 2024
The Third Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, China.
Background: Myocardial ischemia/reperfusion (MI/R) injury is the main cause of death worldwide and poses a significant threat to cardiac health. Ginsenoside Rg1 has been shown to have inhibitory effects on inflammatory activation, oxidative stress, and cardiac injury, suggesting that Rg1 may have therapeutic effects on MI/R injury. However, the mechanism remains to be further studied.
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